Thrombosis, a leading contributor to global health burden, is a complex process involving the interplay of various cell types, including vascular endothelial cells, platelets, and red blood cells. Oxidative stress, characterized by an overproduction of reactive oxygen species (ROS), can significantly impair the function of these cells, thus instigating a cascade of events leading to thrombus formation. In this review, we comprehensively explore the role of oxidative stress within these cells, and its mechanistic contribution to thrombogenesis, and the application of oxidative therapy in inhibiting thrombosis. By dissecting the intricacies of oxidative stress and its impact on thrombosis, we underscore its potential as a viable therapeutic target. Therefore, further research in this direction is warranted to enhance our understanding and management of thrombotic disorders.
Keyphrases
- oxidative stress
- induced apoptosis
- pulmonary embolism
- dna damage
- reactive oxygen species
- global health
- signaling pathway
- endoplasmic reticulum stress
- red blood cell
- endothelial cells
- diabetic rats
- ischemia reperfusion injury
- cell cycle arrest
- public health
- single cell
- stem cells
- mesenchymal stem cells
- bone marrow
- cell proliferation